Approach to Shunts Intracardiac Shunts An intracardiac shunt results from an abnormal communication between the pulmonary and systemic circulations at the level of the heart, which results in mixing of venous and arterial blood. Shunting occurs from the higher pressure system to the lower pressure system. Isolated intracardiac communications [atrial septal defects (ASDs) and ventricular septal defects (VSDs)] typically result in left-to-right flow and may elude detection for many years. Conversely, intracardiac communications resulting in right-to-left flow are detected earlier due to the presence of cyanosis. Longstanding left-to-right shunts can increase the right-sided pressures and therefore eventually result in reversal of flow through the shunt and then cause cyanosis (Eisenmenger syndrome). Intracardiac shunts may be congenital or acquired with congenital defects resulting from abnormal morphogenesis of the atrial or ventricular septa. Intracardiac shunts are the most common congenital heart defects. Acquired shunts result from ischemia, trauma, infection, or iatrogenesis. Although shunts are typically first detected and characterized by echocardiography, the role of cardiac MR and cardiac CT continues to grow. Both CT and MR have good spatial resolution to comprehensively characterize the shunt, their relationship with other anatomical structures, and detection of associated anomalies. With the use of phase-contrast imaging on cardiac MR, blood can be reliably quantified in the systemic and pulmonary systems, allowing determination of the degree of shunting. Cardiac MR can also accurately quantify ventricular volumes and function with CT used when there is a contraindication for MR. A pulmonary to systemic flow ratio (Qp:Qs) > 1.5 is considered significant and can result in right heart overload and failure. Cardiac CT does not allow direct flow quantification and exposes the patient to ionizing radiation; therefore, it is used mainly for morphological evaluation of shunts or when other imaging modalities are limited or unavailable. Treatment options depend on multiple factors, including the patient’s symptoms, ventricular volumes and function, pulmonary arterial pressure, Qp:Qs ratio, location of the defect, size of the defect and surrounding septa, the number of defects, associated anomalies, and others. Types of Intracardiac Shunts Atrial Septal Defects ASDs result from abnormal communication at the level of the atria. They may be single or multiple and can vary in size and shape. Based on location, an ASD can be classified as ostium secundum, ostium primum, sinus venosus, or coronary sinus. ASDs result in enlargement of the right atrium, right ventricle, and pulmonary arteries. Ostium secundum ASD is the most common type of and accounts for 75% of all ASDs. This defect is centered in the fossa ovalis and results from excessive apoptosis of the septum primum or incomplete formation of the septum secundum. This results in a permanent interatrial communication. This is unlike a patent foramen ovale (PFO), which is a persistent fetal interatrial communication into adulthood. In cases of a PFO, there is normal development of the septum primum flap and septum secundum; however, there is lack of fusion of these 2 structures, resulting in interatrial communication. Ostium primum ASD accounts for 15-20% of ASDs. This defect is considered the mildest form of an endocardial cushion defect and results from failed fusion between the free edge of the septum primum and the atrioventricular cushions. This defect is located immediately adjacent to the mitral valve annulus. Sinus venosus ASD accounts for 5-10% of all ASDs. This defect is located either in the superior interatrial septum or in the inferior interatrial septum. A superior sinus venosus ASD is typically associated with partial anomalous pulmonary venous return of the right upper &/or right middle lobe into the superior vena cava. An inferior sinus venosus ASD may be associated with partial anomalous pulmonary venous return to the intrapericardial segment of the inferior vena cava or right atrium. Unroofed coronary sinus ASD is the rarest type of ASD and accounts for < 1% of all ASDs. This defect results from abnormal septation between the left atrium and the adjacent coronary sinus. This results in shunting at the atrial level through the coronary sinus (left atrium to coronary sinus to right atrium) and is therefore considered a form of ASD. It is associated with a left-sided superior vena cava. Ventricular Septal Defects VSDs result from abnormal communication at the level of the ventricles. These defects are the most common congenital abnormality found in children and may close spontaneously in a large percentage of patients. VSDs may be single or multiple and can vary in size and shape. Depending on their location, they can be classified as perimembranous, subarterial/outflow, muscular, and inflow. VSDs result in enlargement of the right ventricle, pulmonary artery, left atrium, and left ventricle. Perimembranous VSD is the most common type and accounts for 80% of all VSDs. This type of defect is located below the crista supraventricularis, anterior to the septal leaflet of the tricuspid valve, and is bounded by muscular and membranous septum. This defect may close spontaneously by apposition of the septal leaflet of the tricuspid valve. Subarterial/outflow VSD accounts for 5% of all VSDs. This defect is located above the crista supraventricularis and is bounded by the fibrous annulus of the semilunar valve &/or muscular tissue. It may be associated with aortic valve prolapse and regurgitation. Muscular VSD accounts for 10% of all VSDs. This defect is located in the trabecular portion of the interventricular septum; therefore, the defect is bounded only by muscle. Inflow VSD accounts for 5% of all VSDs and is almost exclusively associated with endocardial cushion defects. This defect is located anterior to the tricuspid valve annulus and extends to the muscular &/or membranous septum. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related posts: page 2: CORONARY ARTERY DISEASE 7: CONGENITAL HEART DISEASE INDEX Multimodality Approach to Cardiovascular Disorders Approach to Heart Failure Stay updated, free articles. Join our Telegram channel Join Tags: CT and MR in Cardiology Apr 6, 2020 | Posted by admin in CARDIOVASCULAR IMAGING | Comments Off on Approach to Shunts Full access? Get Clinical Tree
Approach to Shunts Intracardiac Shunts An intracardiac shunt results from an abnormal communication between the pulmonary and systemic circulations at the level of the heart, which results in mixing of venous and arterial blood. Shunting occurs from the higher pressure system to the lower pressure system. Isolated intracardiac communications [atrial septal defects (ASDs) and ventricular septal defects (VSDs)] typically result in left-to-right flow and may elude detection for many years. Conversely, intracardiac communications resulting in right-to-left flow are detected earlier due to the presence of cyanosis. Longstanding left-to-right shunts can increase the right-sided pressures and therefore eventually result in reversal of flow through the shunt and then cause cyanosis (Eisenmenger syndrome). Intracardiac shunts may be congenital or acquired with congenital defects resulting from abnormal morphogenesis of the atrial or ventricular septa. Intracardiac shunts are the most common congenital heart defects. Acquired shunts result from ischemia, trauma, infection, or iatrogenesis. Although shunts are typically first detected and characterized by echocardiography, the role of cardiac MR and cardiac CT continues to grow. Both CT and MR have good spatial resolution to comprehensively characterize the shunt, their relationship with other anatomical structures, and detection of associated anomalies. With the use of phase-contrast imaging on cardiac MR, blood can be reliably quantified in the systemic and pulmonary systems, allowing determination of the degree of shunting. Cardiac MR can also accurately quantify ventricular volumes and function with CT used when there is a contraindication for MR. A pulmonary to systemic flow ratio (Qp:Qs) > 1.5 is considered significant and can result in right heart overload and failure. Cardiac CT does not allow direct flow quantification and exposes the patient to ionizing radiation; therefore, it is used mainly for morphological evaluation of shunts or when other imaging modalities are limited or unavailable. Treatment options depend on multiple factors, including the patient’s symptoms, ventricular volumes and function, pulmonary arterial pressure, Qp:Qs ratio, location of the defect, size of the defect and surrounding septa, the number of defects, associated anomalies, and others. Types of Intracardiac Shunts Atrial Septal Defects ASDs result from abnormal communication at the level of the atria. They may be single or multiple and can vary in size and shape. Based on location, an ASD can be classified as ostium secundum, ostium primum, sinus venosus, or coronary sinus. ASDs result in enlargement of the right atrium, right ventricle, and pulmonary arteries. Ostium secundum ASD is the most common type of and accounts for 75% of all ASDs. This defect is centered in the fossa ovalis and results from excessive apoptosis of the septum primum or incomplete formation of the septum secundum. This results in a permanent interatrial communication. This is unlike a patent foramen ovale (PFO), which is a persistent fetal interatrial communication into adulthood. In cases of a PFO, there is normal development of the septum primum flap and septum secundum; however, there is lack of fusion of these 2 structures, resulting in interatrial communication. Ostium primum ASD accounts for 15-20% of ASDs. This defect is considered the mildest form of an endocardial cushion defect and results from failed fusion between the free edge of the septum primum and the atrioventricular cushions. This defect is located immediately adjacent to the mitral valve annulus. Sinus venosus ASD accounts for 5-10% of all ASDs. This defect is located either in the superior interatrial septum or in the inferior interatrial septum. A superior sinus venosus ASD is typically associated with partial anomalous pulmonary venous return of the right upper &/or right middle lobe into the superior vena cava. An inferior sinus venosus ASD may be associated with partial anomalous pulmonary venous return to the intrapericardial segment of the inferior vena cava or right atrium. Unroofed coronary sinus ASD is the rarest type of ASD and accounts for < 1% of all ASDs. This defect results from abnormal septation between the left atrium and the adjacent coronary sinus. This results in shunting at the atrial level through the coronary sinus (left atrium to coronary sinus to right atrium) and is therefore considered a form of ASD. It is associated with a left-sided superior vena cava. Ventricular Septal Defects VSDs result from abnormal communication at the level of the ventricles. These defects are the most common congenital abnormality found in children and may close spontaneously in a large percentage of patients. VSDs may be single or multiple and can vary in size and shape. Depending on their location, they can be classified as perimembranous, subarterial/outflow, muscular, and inflow. VSDs result in enlargement of the right ventricle, pulmonary artery, left atrium, and left ventricle. Perimembranous VSD is the most common type and accounts for 80% of all VSDs. This type of defect is located below the crista supraventricularis, anterior to the septal leaflet of the tricuspid valve, and is bounded by muscular and membranous septum. This defect may close spontaneously by apposition of the septal leaflet of the tricuspid valve. Subarterial/outflow VSD accounts for 5% of all VSDs. This defect is located above the crista supraventricularis and is bounded by the fibrous annulus of the semilunar valve &/or muscular tissue. It may be associated with aortic valve prolapse and regurgitation. Muscular VSD accounts for 10% of all VSDs. This defect is located in the trabecular portion of the interventricular septum; therefore, the defect is bounded only by muscle. Inflow VSD accounts for 5% of all VSDs and is almost exclusively associated with endocardial cushion defects. This defect is located anterior to the tricuspid valve annulus and extends to the muscular &/or membranous septum. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related posts: page 2: CORONARY ARTERY DISEASE 7: CONGENITAL HEART DISEASE INDEX Multimodality Approach to Cardiovascular Disorders Approach to Heart Failure Stay updated, free articles. Join our Telegram channel Join Tags: CT and MR in Cardiology Apr 6, 2020 | Posted by admin in CARDIOVASCULAR IMAGING | Comments Off on Approach to Shunts Full access? Get Clinical Tree
